Changzhou Kangpu Pharmaceutical Co., Ltd.
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Founded in:
1979-12-01 -
Country:
China -
Address:
No. 6, Jingde East Road, Qianhuang Town, Wujin District -
Tax NO.:
91320412250816627K -
Registered Funds:
20 million yuan -
Website:
-
Email:
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Sulpiride |
This product belongs to the benzamide antipsychotic drug. Its characteristic action is to selectively block the dopamine (DA2) receptors of the mesolimbic system, with little effect on other neurotransmitter receptors, mild anticholinergic effect, and no obvious sedative and anti-excitement and agitation effects. This product also has strong antiemetic and gastric juice secretion inhibitory effects.
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This product belongs to the benzamide antipsychotic drug. Its characteristic action is to selectively block the dopamine (DA2) receptors of the mesolimbic system, with little effect on other neurotransmitter receptors, mild anticholinergic effect, and no obvious sedative and anti-excitement and agitation effects. This product also has strong antiemetic and gastric juice secretion inhibitory effects. |
15676-16-1 | 11 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Carbamazepine |
Anticonvulsant, anti-epileptic, anti-neuropathic pain, anti-manic-depressive, improves the symptoms of certain mental illnesses, and treats central diabetes insipidus; possible mechanisms include use-dependent blocking of various excitable cell membrane Na channels, inhibition of T-type calcium channels, enhancement of central noradrenergic nerve activity, promotion of antidiuretic hormone (ADH) secretion, or increased sensitivity of effectors to ADH.
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Anticonvulsant, anti-epileptic, anti-neuropathic pain, anti-manic-depressive, improves the symptoms of certain mental illnesses, and treats central diabetes insipidus; possible mechanisms include use-dependent blocking of various excitable cell membrane Na channels, inhibition of T-type calcium channels, enhancement of central noradrenergic nerve activity, promotion of antidiuretic hormone (ADH) secretion, or increased sensitivity of effectors to ADH. |
298-46-4 | 43 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Propanolol |
1. It non-selectively competitively inhibits adrenaline beta receptor blockers, reduces the contractile force and contractile speed of the heart, inhibits the contraction of vascular smooth muscle, reduces myocardial oxygen consumption, and is used to treat angina pectoris; 2. It inhibits the adrenergic excitement of the cardiac pacemaker potential and is used to treat arrhythmias; 3. It inhibits the release of renin and reduces cardiac output through central and adrenergic neuron blocking, and is used to treat hypertension; 4. It competitively antagonizes the effects of isoproterenol and norepinephrine, blocks beta 2 receptors, reduces plasma renin activity, has embryotoxicity, may cause bronchospasm, inhibits insulin secretion to increase blood sugar, masks hypoglycemia symptoms, and delays the recovery of hypoglycemia; 5. It has obvious anti-platelet aggregation effect.
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1. It non-selectively competitively inhibits adrenaline beta receptor blockers, reduces the contractile force and contractile speed of the heart, inhibits the contraction of vascular smooth muscle, reduces myocardial oxygen consumption, and is used to treat angina pectoris; 2. It inhibits the adrenergic excitement of the cardiac pacemaker potential and is used to treat arrhythmias; 3. It inhibits the release of renin and reduces cardiac output through central and adrenergic neuron blocking, and is used to treat hypertension; 4. It competitively antagonizes the effects of isoproterenol and norepinephrine, blocks beta 2 receptors, reduces plasma renin activity, has embryotoxicity, may cause bronchospasm, inhibits insulin secretion to increase blood sugar, masks hypoglycemia symptoms, and delays the recovery of hypoglycemia; 5. It has obvious anti-platelet aggregation effect. |
525-66-6 | 0 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Phenylbutazone |
This product is a non-steroidal anti-inflammatory drug with a strong anti-inflammatory effect, a good effect on inflammatory pain, and a role in promoting uric acid excretion, but a weak antipyretic effect.
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This product is a non-steroidal anti-inflammatory drug with a strong anti-inflammatory effect, a good effect on inflammatory pain, and a role in promoting uric acid excretion, but a weak antipyretic effect. |
50-33-9 | 10 |
| Name | Description | Content | CAS NO. | Registered Holders |
|---|---|---|---|---|
| Phenytoin sodium |
Antiepileptic drugs, antiarrhythmic drugs. The therapeutic dose does not cause sedation and hypnosis, and has a selective antagonistic effect on the tonic phase of super-strong electric shock and convulsion, but is ineffective or even aggravates the spasm phase. Therefore, it is effective for grand mal epileptic seizures, but ineffective for absence seizures. Its antiepileptic mechanism is generally believed to increase the outflow of sodium ions from cells, reduce the inflow of sodium ions, stabilize the nerve cell membrane, increase the excitation threshold, and reduce the spread of high-frequency discharges in the lesion. In addition, this product shortens the action potential interval and the effective refractory period, and can also inhibit the influx of calcium ions, reduce myocardial autonomy, inhibit the sympathetic center, and have an inhibitory effect on the ectopic rhythm points of the atria and ventricles, and increase the thresholds for atrial fibrillation and ventricular fibrillation.
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Antiepileptic drugs, antiarrhythmic drugs. The therapeutic dose does not cause sedation and hypnosis, and has a selective antagonistic effect on the tonic phase of super-strong electric shock and convulsion, but is ineffective or even aggravates the spasm phase. Therefore, it is effective for grand mal epileptic seizures, but ineffective for absence seizures. Its antiepileptic mechanism is generally believed to increase the outflow of sodium ions from cells, reduce the inflow of sodium ions, stabilize the nerve cell membrane, increase the excitation threshold, and reduce the spread of high-frequency discharges in the lesion. In addition, this product shortens the action potential interval and the effective refractory period, and can also inhibit the influx of calcium ions, reduce myocardial autonomy, inhibit the sympathetic center, and have an inhibitory effect on the ectopic rhythm points of the atria and ventricles, and increase the thresholds for atrial fibrillation and ventricular fibrillation. |
630-93-3 | 14 |